+publisher:"University of North Carolina" +contributor:("Matson, Steven")

University of North Carolina

1. LaFave, Matthew. Detection and Analysis of Common Fragile Sites in Drosophila melanogaster.

Degree: 2011, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:775a4a60-f95d-4fc7-b1b6-a5fe39c6f48c

► Common fragile sites (CFSs) are regions of DNA exceptionally prone to breakage. While these regions have implications in cancer, the causes of chromosome fragility remain… (more)

▼ Common fragile sites (CFSs) are regions of DNA exceptionally prone to breakage. While these regions have implications in cancer, the causes of chromosome fragility remain poorly understood. This is partially due to relatively low-resolution cytological mapping of CFSs, and the use of exogenous agents to induce chromosome breakage. In an effort to better understand the causes of fragility, I have developed Drosophila melanogaster as a model for CFS study. In doing so, I have developed approaches to identify CFSs at a high resolution, based on both spontaneous chromosomal events and breakage induced by the inhibition of replication. In the first approach, I used a mutant form of mus309, the ortholog of human BLM helicase, to locate CFSs by visualizing sites of DNA breakage as mitotic crossovers. High rates of breakage correspond to CFSs, and results from my study indicate that there is a significantly non-uniform rate of mitotic crossovers across the left arm of chromosome 2. This work constitutes the first report of specific regions sensitive to endogenous damage in D. melanogaster. Further, the resolution of damage detection can be brought even higher with SNP mapping. My second approach is a novel assay that uses S2 cell culture to detect preferential sites of exogenous DNA integration, a hallmark of CFSs. This allows me to survey the entire genome, while using high-throughput sequencing to obtain a resolution of CFS detection orders of magnitude better than previous studies. I obtained numerous integration events under a variety of conditions, providing evidence of putative fragile regions. I anticipate that the assays I developed will serve as valuable tools for the detection of DNA breakage in future studies. Further, I expect the characterization of the CFSs detected from both of these approaches will lead to a better understanding of the causes of inherent genome instability. Advisors/Committee Members: LaFave, Matthew, Sekelsky, Jeff, Ahmed, Shawn, Jones, Corbin, Matson, Steven, Ramsden, Dale.

Subjects/Keywords: School of Medicine; Curriculum in Genetics and Molecular Biology

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APA (6^th Edition):

LaFave, M. (2011). Detection and Analysis of Common Fragile Sites in Drosophila melanogaster. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:775a4a60-f95d-4fc7-b1b6-a5fe39c6f48c

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

LaFave, Matthew. “Detection and Analysis of Common Fragile Sites in Drosophila melanogaster.” 2011. Thesis, University of North Carolina. Accessed January 19, 2021. https://cdr.lib.unc.edu/record/uuid:775a4a60-f95d-4fc7-b1b6-a5fe39c6f48c.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

LaFave, Matthew. “Detection and Analysis of Common Fragile Sites in Drosophila melanogaster.” 2011. Web. 19 Jan 2021.

Vancouver:

LaFave M. Detection and Analysis of Common Fragile Sites in Drosophila melanogaster. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2021 Jan 19]. Available from: https://cdr.lib.unc.edu/record/uuid:775a4a60-f95d-4fc7-b1b6-a5fe39c6f48c.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

LaFave M. Detection and Analysis of Common Fragile Sites in Drosophila melanogaster. [Thesis]. University of North Carolina; 2011. Available from: https://cdr.lib.unc.edu/record/uuid:775a4a60-f95d-4fc7-b1b6-a5fe39c6f48c

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Carolina

2. Romero, Noelle-Erin. Biochemical Activities and Genetic Functions of the Drosophila melanogaster FANCM Helicase in DNA Repair.

Degree: 2016, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:67fec902-fa62-4b39-bb59-d61616a6b05e

► The DNA damage response in eukaryotes involves multiple, complex, and often redundant pathways that respond to various types of DNA damage that affect one or… (more)

▼ The DNA damage response in eukaryotes involves multiple, complex, and often redundant pathways that respond to various types of DNA damage that affect one or both strands of DNA. One type of toxic DNA damage that can occur is a double-strand break (DSB). Repair of a DSB can lead to the formation of a recombination product known as a crossover (CO). Crossovers in mitotic cells can be deleterious and lead to chromosomal rearrangements or cell death. In order to limit crossing over during DSB repair, eukaryotes possess mechanisms to ensure crossovers do not occur. In this manner, several helicases function during repair of DSBs to promote accurate repair and prevent the formation of crossovers through homologous recombination. Among these helicases is the Fanconi anemia group M (FANCM) protein. FANCM is one of 17 Fanconi anemia (FA) proteins and is one of the most broadly? conserved FA proteins. FANCM and its orthologs, Mph1 and Fml1, are DNA junction-specific helicases/translocases that process homologous recombination (HR) intermediates. Additionally, FANCM has been implicated in a number of DNA metabolic processes including activation of the S-phase checkpoint, trasversal of interstrand crosslinks, recruitment of the proteins such as the FA core complex and Blm to sites of DNA damage, and prevention of mitotic crossovers during double-strand break repair. The helicase activity of FANCM is believed to be important in crossover prevention, but no helicase activity has been detected in vitro. I report here a genetic and biochemical study of Drosophila melanogaster Fancm. I show that purified Fancm is a 3ʹ to 5ʹ ATP-dependent helicase that can disassemble recombination intermediates, but only through limited lengths of duplex DNA. Using transgenic flies expressing full-length or truncated Fancm, each with either a wild-type or mutated helicase domain, I found that there are helicase-independent and C-terminus independent functions in responding to DNA damage and in preventing mitotic crossovers. Advisors/Committee Members: Romero, Noelle-Erin, Matson, Steven, Sekelsky, Jeff, Erie, Dorothy, Duronio, Robert, Vaziri, Cyrus.

Subjects/Keywords: School of Medicine; Curriculum in Genetics and Molecular Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Romero, N. (2016). Biochemical Activities and Genetic Functions of the Drosophila melanogaster FANCM Helicase in DNA Repair. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:67fec902-fa62-4b39-bb59-d61616a6b05e

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Romero, Noelle-Erin. “Biochemical Activities and Genetic Functions of the Drosophila melanogaster FANCM Helicase in DNA Repair.” 2016. Thesis, University of North Carolina. Accessed January 19, 2021. https://cdr.lib.unc.edu/record/uuid:67fec902-fa62-4b39-bb59-d61616a6b05e.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Romero, Noelle-Erin. “Biochemical Activities and Genetic Functions of the Drosophila melanogaster FANCM Helicase in DNA Repair.” 2016. Web. 19 Jan 2021.

Vancouver:

Romero N. Biochemical Activities and Genetic Functions of the Drosophila melanogaster FANCM Helicase in DNA Repair. [Internet] [Thesis]. University of North Carolina; 2016. [cited 2021 Jan 19]. Available from: https://cdr.lib.unc.edu/record/uuid:67fec902-fa62-4b39-bb59-d61616a6b05e.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Romero N. Biochemical Activities and Genetic Functions of the Drosophila melanogaster FANCM Helicase in DNA Repair. [Thesis]. University of North Carolina; 2016. Available from: https://cdr.lib.unc.edu/record/uuid:67fec902-fa62-4b39-bb59-d61616a6b05e

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Carolina

3. Meiners, Matthew. THE MECHANISM OF MODULATION OF THE ESCHERICHIA COLI DNA HELICASE II (UVRD) UNWINDING ACTIVITY, A STUDY OF THE 2B SUBDOMAIN.

Degree: Biology, 2014, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:854a3b1d-cf4c-4a19-90d1-f3893c2600b5

► Helicases are ubiquitous motor proteins which catalyze the separation of double stranded DNA into single stranded DNA for the purposes of replication, recombination and repair.… (more)

▼ Helicases are ubiquitous motor proteins which catalyze the separation of double stranded DNA into single stranded DNA for the purposes of replication, recombination and repair. Escherichia coli DNA helicase II, also known as UvrD, is a Superfamily 1 helicase involved in post-replicative mismatch repair, nucleotide excision repair and conjugative recombination. These roles that UvrD fills in the cell require dramatically different unwinding activities to be performed accurately. Nucleotide excision repair only requires a 12-13 bp section of DNA to be unwound for efficient repair, while methyl-directed mismatch repair and recombination can require upwards of 1 kilobase of DNA to be traversed for the processes to be faithfully completed. These contrasting activity requirements are even more confusing when one examines the in vitro processivity of UvrD, which has been measured to be on the order of 40 of bp unwound in a single event. This begs the question how is the activity of UvrD regulated to perform these roles which require converse activity levels in the cell? This dissertation offers evidence that the 2B subdomain of UvrD is involved in modulating the activity of the helicase. Mutations within this subdomain have been linked to dramatically stimulated helicase activity which I have shown is due to an increase in the processivity of the unwinding reaction. In addition, the data presented here suggest that this subdomain is the interaction site between UvrD and other proteins which have been shown to have a stimulatory effect on the unwinding activity of UvrD. However, deletion of this subdomain in its entirety does not seem to stimulate the helicase activity of UvrD as it has been shown to do in other Superfamily 1 helicases. It can be concluded that the 2B subdomain plays a poorly understood role in regulating the unwinding activity of UvrD and this work offers an exploratory look in to the rolesthis subdomain performs in the regulation of the helicase. Advisors/Committee Members: Meiners, Matthew, Matson, Steven, Erie, Dorothy, Copenhaver, Gregory, Sekelsky, Jeff, Kunkel, Tom.

Subjects/Keywords: Molecular biology; Biochemistry; College of Arts and Sciences; Department of Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Meiners, M. (2014). THE MECHANISM OF MODULATION OF THE ESCHERICHIA COLI DNA HELICASE II (UVRD) UNWINDING ACTIVITY, A STUDY OF THE 2B SUBDOMAIN. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:854a3b1d-cf4c-4a19-90d1-f3893c2600b5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Meiners, Matthew. “THE MECHANISM OF MODULATION OF THE ESCHERICHIA COLI DNA HELICASE II (UVRD) UNWINDING ACTIVITY, A STUDY OF THE 2B SUBDOMAIN.” 2014. Thesis, University of North Carolina. Accessed January 19, 2021. https://cdr.lib.unc.edu/record/uuid:854a3b1d-cf4c-4a19-90d1-f3893c2600b5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Meiners, Matthew. “THE MECHANISM OF MODULATION OF THE ESCHERICHIA COLI DNA HELICASE II (UVRD) UNWINDING ACTIVITY, A STUDY OF THE 2B SUBDOMAIN.” 2014. Web. 19 Jan 2021.

Vancouver:

Meiners M. THE MECHANISM OF MODULATION OF THE ESCHERICHIA COLI DNA HELICASE II (UVRD) UNWINDING ACTIVITY, A STUDY OF THE 2B SUBDOMAIN. [Internet] [Thesis]. University of North Carolina; 2014. [cited 2021 Jan 19]. Available from: https://cdr.lib.unc.edu/record/uuid:854a3b1d-cf4c-4a19-90d1-f3893c2600b5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Meiners M. THE MECHANISM OF MODULATION OF THE ESCHERICHIA COLI DNA HELICASE II (UVRD) UNWINDING ACTIVITY, A STUDY OF THE 2B SUBDOMAIN. [Thesis]. University of North Carolina; 2014. Available from: https://cdr.lib.unc.edu/record/uuid:854a3b1d-cf4c-4a19-90d1-f3893c2600b5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Carolina

4. Monroe, Danny Scott. Hmi1p and UvrD: Two Superfamily I helicases and their respective roles in S. cerevisiae mtDNA maintenance and E. coli methyl-directed mismatch repair.

Degree: Biology, 2008, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:d85a55cc-6c89-4b27-a909-916c3d77afc5

► Helicases are vital to all aspects of genomic maintenance. Double-stranded DNA, DNA/RNA hybrids, and self-annealed RNA require the action of this class of proteins to… (more)

Subjects/Keywords: College of Arts and Sciences; Department of Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Monroe, D. S. (2008). Hmi1p and UvrD: Two Superfamily I helicases and their respective roles in S. cerevisiae mtDNA maintenance and E. coli methyl-directed mismatch repair. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:d85a55cc-6c89-4b27-a909-916c3d77afc5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Monroe, Danny Scott. “Hmi1p and UvrD: Two Superfamily I helicases and their respective roles in S. cerevisiae mtDNA maintenance and E. coli methyl-directed mismatch repair.” 2008. Thesis, University of North Carolina. Accessed January 19, 2021. https://cdr.lib.unc.edu/record/uuid:d85a55cc-6c89-4b27-a909-916c3d77afc5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Monroe, Danny Scott. “Hmi1p and UvrD: Two Superfamily I helicases and their respective roles in S. cerevisiae mtDNA maintenance and E. coli methyl-directed mismatch repair.” 2008. Web. 19 Jan 2021.

Vancouver:

Monroe DS. Hmi1p and UvrD: Two Superfamily I helicases and their respective roles in S. cerevisiae mtDNA maintenance and E. coli methyl-directed mismatch repair. [Internet] [Thesis]. University of North Carolina; 2008. [cited 2021 Jan 19]. Available from: https://cdr.lib.unc.edu/record/uuid:d85a55cc-6c89-4b27-a909-916c3d77afc5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Monroe DS. Hmi1p and UvrD: Two Superfamily I helicases and their respective roles in S. cerevisiae mtDNA maintenance and E. coli methyl-directed mismatch repair. [Thesis]. University of North Carolina; 2008. Available from: https://cdr.lib.unc.edu/record/uuid:d85a55cc-6c89-4b27-a909-916c3d77afc5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Carolina

5. Robertson, Adam Brian. MutL involvement in two DNA repair pathways: methyl-directed mismatch repair and very short patch repair.

Degree: Biology, 2007, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:f0d64b7d-3e84-42e2-bf79-d42941754e26

► MutL is an essential component of the Escherichia coli mismatch repair (MMR) pathway and has been shown to interact with nearly every protein involved in… (more)

▼ MutL is an essential component of the Escherichia coli mismatch repair (MMR) pathway and has been shown to interact with nearly every protein involved in the MMR pathway including MutS, MutH and UvrD. The DNA binding properties of MutL in MMR have been controversial for nearly two decades. The DNA binding requirement by MutL was addressed using a point mutant of MutL—MutL-R266E—which binds DNA poorly. Our results demonstrate, using data obtained from biochemical and genetic analyses with MutL-R266E, that MutL must bind DNA to function in MMR. Therefore, we have attempted to resolve the controversial issue regarding the DNA binding properties of MutL. MutL is thought to be the master coordinator of MMR, accomplishing this regulatory role through its ATP binding, hydrolysis, and release cycle. Using a point mutant of MutL that cannot bind ATP—MutL-D58A, we show that this mutant is unable to interact with MutS, and MutH and UvrD. Additionally, we have identified the step in MMR that MutL must hydrolyze its bound ATP in order to continue its normal function in MMR. We accomplished this using another point mutant of MutL that cannot hydrolyze ATP—MutL-E29A. These results lend support for the hypothesis of temporal regulation of MMR by the MutL ATPase. Using MutL-E29A and MutL-D58A in biochemical and genetic assays, we have attempted to identify a role for the MutL ATPase in MMR. These data suggest that MutL must be bound to ATP to function in MMR prior to the loading of the UvrD helicase. Additionally, these data implicate ATP hydrolysis by MutL at a step in the MMR pathway after the UvrD helicase is loaded onto the DNA by MutL. Previous studies have shown that MutL serves to augment the repair efficiency of the very short patch (VSP) repair pathway. We have reconstituted the minimal VSP repair pathway in vitro. We suggest a biochemical role for MutL in VSP repair. The reconstitution of this system will allow further studies addressing the function of MutL in VSP repair. Advisors/Committee Members: Robertson, Adam Brian, Matson, Steven, University of North Carolina at Chapel Hill.

Subjects/Keywords: College of Arts and Sciences; Department of Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Robertson, A. B. (2007). MutL involvement in two DNA repair pathways: methyl-directed mismatch repair and very short patch repair. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:f0d64b7d-3e84-42e2-bf79-d42941754e26

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Robertson, Adam Brian. “MutL involvement in two DNA repair pathways: methyl-directed mismatch repair and very short patch repair.” 2007. Thesis, University of North Carolina. Accessed January 19, 2021. https://cdr.lib.unc.edu/record/uuid:f0d64b7d-3e84-42e2-bf79-d42941754e26.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Robertson, Adam Brian. “MutL involvement in two DNA repair pathways: methyl-directed mismatch repair and very short patch repair.” 2007. Web. 19 Jan 2021.

Vancouver:

Robertson AB. MutL involvement in two DNA repair pathways: methyl-directed mismatch repair and very short patch repair. [Internet] [Thesis]. University of North Carolina; 2007. [cited 2021 Jan 19]. Available from: https://cdr.lib.unc.edu/record/uuid:f0d64b7d-3e84-42e2-bf79-d42941754e26.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Robertson AB. MutL involvement in two DNA repair pathways: methyl-directed mismatch repair and very short patch repair. [Thesis]. University of North Carolina; 2007. Available from: https://cdr.lib.unc.edu/record/uuid:f0d64b7d-3e84-42e2-bf79-d42941754e26

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Carolina

6. Lujan, Scott. Bacterial Conjugation and its Inhibition: The Hows and Whys of Conjugation and What Can be Done to Control It.

Degree: Biochemistry and Biophysics, 2008, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:479d9a87-b137-4371-b5de-c871ab80e258

► Conjugation is the primary vehicle for the horizontal transfer virulence factor genes, such as antibiotic resistance, within and between bacterial strains. In certain epicenters, such… (more)

▼ Conjugation is the primary vehicle for the horizontal transfer virulence factor genes, such as antibiotic resistance, within and between bacterial strains. In certain epicenters, such as hospitals in less developed parts of the world, immune-compromised patients and misuse of antibiotics combine to select for the development and dissemination of these pathogenicity factors via conjugation. Inhibition of conjugation would prove a boon for curbing the creation and spread of new virulent or multi-drug resistant strains. DNA relaxases are the keystone proteins of each conjugative system. TraI is the relaxase of the F plasmid, the archetypal model system for conjugation. Toward revelation and inhibition of relaxase mechanisms, I used bioinformatics and limited proteolysis to find and identify new domains on the F TraI enzyme. I then solved TraI/DNA co-crystal structures that showed a novel DNA binding mode. Based on structure comparisons, sequence conservation, and mutant activity studies, I proposed a mechanism for TraI activity that required the existence of a dual phosphotyrosine intermediate, which has since been observed. I then demonstrated that bisphosphonate compounds mimicking this intermediate are nanomolar in vitro TraI inhibitors. I determined the relaxase structure in complex with one such inhibitor, bound as predicted. We showed that several of these compounds are potent in cell inhibitors of conjugation that often selectively kill conjugation-capable cells, a novel antibiotic paradigm. We showed that oral treatment of gnotobiotic mice with two inhibitors, clodronate and etidronate, decreased the gastrointestinal F+ bacterial load twentyfold without apparent side effects. Beyond the model system, etidronate showed selective in cell potency versus cells harboring a known clinical resistance-bearing R100 plasmid. Etidronate and clodronate are already clinically approved for the treatment of bone loss in humans. Toward more general relaxase inhibition phylogenetic analyses and studies with other medically relevant relaxases, including viral replicative relaxases, are ongoing. Advisors/Committee Members: Lujan, Scott, Redinbo, Matthew R., Wolfenden, Richard, Pielak, Gary J., Matson, Steven, Temple, Brenda.

Subjects/Keywords: School of Medicine; Department of Biochemistry and Biophysics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lujan, S. (2008). Bacterial Conjugation and its Inhibition: The Hows and Whys of Conjugation and What Can be Done to Control It. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:479d9a87-b137-4371-b5de-c871ab80e258

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lujan, Scott. “Bacterial Conjugation and its Inhibition: The Hows and Whys of Conjugation and What Can be Done to Control It.” 2008. Thesis, University of North Carolina. Accessed January 19, 2021. https://cdr.lib.unc.edu/record/uuid:479d9a87-b137-4371-b5de-c871ab80e258.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lujan, Scott. “Bacterial Conjugation and its Inhibition: The Hows and Whys of Conjugation and What Can be Done to Control It.” 2008. Web. 19 Jan 2021.

Vancouver:

Lujan S. Bacterial Conjugation and its Inhibition: The Hows and Whys of Conjugation and What Can be Done to Control It. [Internet] [Thesis]. University of North Carolina; 2008. [cited 2021 Jan 19]. Available from: https://cdr.lib.unc.edu/record/uuid:479d9a87-b137-4371-b5de-c871ab80e258.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lujan S. Bacterial Conjugation and its Inhibition: The Hows and Whys of Conjugation and What Can be Done to Control It. [Thesis]. University of North Carolina; 2008. Available from: https://cdr.lib.unc.edu/record/uuid:479d9a87-b137-4371-b5de-c871ab80e258

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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